Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Bone & Calcium Disorders > Flashcards

Bone & Calcium Disorders Flashcards

1
Q

Define osteoporosis

A

Progressive systemic skeletal disease characterised by low bone mass & micro-architectural deterioration of bone tissue leading to increased bone fragility and susceptibility to fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens to bone as you get older?

A

decreased trabecular thickens, decreased connections between vertical trabecular & decreased trabecular strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the 4 key steps in bone remodelling

A
  1. Osteoclast precursors are stimulated by RANKL which is unregulated by vit D, parathyroid & IL II
  2. Osteoclast activity removes bone
  3. Cytokines released inhibit osteoclasts & stimulate osteoblasts
  4. Osteoblasts synthesise osteoid which becomes mineralised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happen to unwanted osteoclasts?

A

Undergo apoptosis due to the influence of oestrogen & bisphosphonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What percentage of women >50 years old are expected to break a bone?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name four common sites of osteoporotic fractures

A
  • neck of femur
  • vertebral body
  • distal radius
  • humeral neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is osteoporosis diagnosed?

A

Bone mass density - DEXA scan of lumbar spine and hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does a DEXA scan calculate?

A

Bone mineral content and density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How can you analyse a DEXA scan?

A

T value compares with young adult
Z value compares with appropriate age
Normal - within 1 SD of young adult reference
Osteopenia - >1SD but <2.5SD below young adult
Osteoporosis >2.5 SD below young adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the relationship between the T score and risk of fracture?

A

Lower the T score the higher the risk of fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Who gets a DEXA scan?

A

Patients >50 years old with low trauma fracture

Patients at increased risk based on risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

State some modifiable risk factors for osteoporosis

A 
Alcohol
BMI 
Exercise 
Smoking 
Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

State some non-modifiable risk factors for osteoporosis

A 
Age
Gender
Ethnicity 
Past Medical History 
Family History
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are people with an increased risk of fracture assessed?

A

Blood tests - FBC U/E, LFTs, TSH
Antibody test if secondary cause suspected
Testosterone levels
Vitamin D and Parathyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What lifestyle advice is given to patients with increased risk of fracture?

A

Strength training/low impact weigh bearing exercise is good. Avoid alcohol and smoking, increase dietary calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name five drug treatments available for osteoporosis

A 
Calcium and Vitamin D Supplements 
Bisphosphonates 
Zoledronic acid 
Denosumab 
Terparatide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do bisphosphonates work?

A

Ingested by osteoclasts leading to cell death and therefore inhibiting bone resorption. Prevents bone loss at vulnerable sites and reduces hip/spine fractures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is zoledronic acid?

A

IV bisphosphonate given in annual infusions for 3 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What portion of patients will have an acute reaction with first infusion of zoledronic acid?

A

1/3rd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the action of Denosumab

A

Monoclonal antibody targets and binds to RANKL to prevent activation and thus osteoclastic activity. Decreases resorption and increases bone density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is denosumab administered?

A

Subcutaneous injection every 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the side effects of denosumab?

A

Hypocalcaemia, eczema, cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the action of Teriparatide

A

Recombinant parathyroid hormone, stimulates bone growth (anabolic agent). Used in severe disease as a daily injection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

On treatment what is the aim for T values

A

= -2.5

Ongoing steroid treatment <1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the direct action of steroids on bone

A

Reduces osteoblast activity and lifespan, suppresses osteoblast precursors and reduces calcium absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the indirect action of steroids on bone

A

Inhibition of gonadal and adrenal steroid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Paget’s disease?

A

Common in elderly, increased bone resorption leads to Increased turnover and abnormal bone is structurally weak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

State the cause of Paget’s disease

A

Genetic + environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which bones are affected by Paget’s?

A

Long bones, pelvis, lumbar spine and skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How will Paget’s present?

A

Pain, deformity, deafness, compression neuropathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What investigations are done on patients with suspected pagets?

A

X-ray, isotope bone scan to show disease distribution, Alk phos usually increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is Paget’s treated?

A

Analgesia and bisphosphonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the pathogenesis of Paget’s disease

A

Abnormal osteoclastic activity followed by increased osteoblastic activity leads to abnormal bone structure, reduced strength and increased risk of fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the difference between monostotic and polystotic?

A

Monostotic - one bone

Polystotic - many bones

35
Q

What is osteogenesis imperfecta?

A

Rare group of genetic disorders from mutations in the COL1A1, COL1A2 collagen type 1 structural genes - most are autosomal dominant inheritance

36
Q

What are the different types of OI?

A

type 1 - mild
type 2 - neonatal (fatal)
type 3/4 - very severe

37
Q

Name the signs associated with OI

A

Blue sclera
Bowing of limbs
Dentinogenesis imperfecta

38
Q

How will severe forms of OI present?

A

In childhood with fractures

39
Q

What must be considered before OI?

A

Non-accidental injury

40
Q

Describe the management of OI

A

No cure only fracture fixation, surgery for deformities and bisphosphonates

41
Q

What happens in response to a fall in plasma calcium?

A

PTH is released from the parathyroid gland

42
Q

Where does PTH act?

A
  • Bone

- Kidneys

43
Q

What does PTH do in the kidneys?

A

-stimulates the enzyme 1alpha hydroxylase to convert 25 hydroxycholecalciferol to 1:25
dihydroxycholecalciferol
- Stimulates calcium and phosphate reabsorption

44
Q

Where does 1:25 dihydroxycholecalciferol come from?

A

Cholesterol in the skin is hit by UV light to form cholecalciferol which moves to the liver to be coverted to 25 hydroxycholecalciferol which is then moved to the kidneys where 1:25 dihydroxycholecalciferol is made under PTH influence

45
Q

What is the effect of the formation of 1:25 dihydroxycholecalciferol?

A
  • stimulates bone breakdown
  • decreases PTH by negative feedback
  • stimulates the gut to increase calcium and phosphate absorption
  • stimulates the kidneys to reabsorb calcium
46
Q

How does PTH act on bone?

A

Causes proliferation of osteoblasts, stimulates RANKL expression and inhibits OPG

47
Q

What is the effect of increased RANKL expression from osteoblasts?

A

Pre-osteoclasts have a RANKL receptor that binds to osteoblasts causing proliferation and differentiation

48
Q

How do osteoclasts help to increase plasma calcium?

A

Type of macrophage that release acid to ‘eat away’ bone thus releasing calcium and phosphate

49
Q

Where is calcitonin released?

A

Thyroid gland

50
Q

What does calcitonin do?

A

Acts to decrease plasma calcium by reducing osteoclast activity and renal reabsorption

51
Q

What are the symptoms of hypercalcaemia?

A 
Bones 
Stones 
Abdominal Groans 
Thrones 
Psychiatric Overtones
52
Q

How will acute hypercalcamia present?

A

Thirst, dehydration, confusion and polyuria

53
Q

How will chronic hypercalcaemia present?

A 
Myopathy/fractures/osteopenia 
Depression 
Hypertension 
Pancreatitis
Renal calculi
54
Q

What causes hypercalcaemia?

A 
Primary hyperparathyroidism 
Malignancy 
Drugs 
Granulomatous disease 
Familial 
MEN 1 and 2
55
Q

How is hypercalcaemia diagnosed?

A

PTH
Urinary Calcium
Cause dependent

56
Q

If PTH is high or normal how do you determine the cause of hypercalcaemia?

A

High urinary calcium - primary or tertiary hyperparathyroidism
Low urinary calcium - FHH

57
Q

In hypercalcaemia what does a low PTH suggest?

A

Bone pathology

58
Q

If PTH is low (bone pathology) how do you determine the cause of hypercalcaemia?

A

High ALP - Mets, Sarcoid, thyrotoxicosis

Low ALP - Myeloma, Vitamin D toxicity, milk-alkali syndrome

59
Q

What is the treatment for acute hypercalcaemia?

A

Fluids 0.9% saline

60
Q

What scan can be used to show the activity of the parathyroid gland?

A

Sestamibi

61
Q

How is hypercalcaemia managed?

A

Depends on cause often surgery or cinacalcet is used

62
Q

What is cinacalet?

A

Mimetic of calcium - tertiary hyperparathyroidism and carcinoma

63
Q

When is a parathyroidectomy indicated?

A

End organ damage
Very high calcium
<50 years old
eEFR <60ml/min

64
Q

State three types of hyperparathyroidism

A

Primary
Secondary
Tertiary

65
Q

Describe primary hyperparathyroidism

A

Overactivity of parathyroid e.g adenoma will present with high calcium and high PTH

66
Q

Describe secondary hyperparathyroidism

A

Physiological response due to low calcium or vitamin D will present with low calcium and high PTH

67
Q

Describe tertiary hyperparathyroidism

A

Due to years of overactivity - becomes autonomous will present with high calcium and PTH

68
Q

What is FHH?

A

Familial hypocalciuric hypercalcaemia

69
Q

Describe FHH

A

Autosomal dominant mutation in the calcium sensing receptor - usually benign and asymptomatic
Diagnosed by hypercalcaemia, decreased urinary calcium excretion and increased PTH

70
Q

What are the signs and symptoms of hypocalcaemia?

A

Parasthesia, muscle cramps/weakness, fatigue, bronchospasm, fits, long QT,
Trousseau sign - carpopedal spasm
Chovsteks sign - twitching of fascia muscles in response to tapping on facial nerve

71
Q

What is given in acute hypocalcaemia?

A

IV calcium gluconate

72
Q

What can cause hypocalcaemia?

A

Hypoparathyroidism
Hypomagnasaemia
Pseudohypoparathyroidism

73
Q

What causes hypoparathyroidism?

A

Congenital absence (DiGeorge Syndrome)
Destruction (surgery/radiotherapy)
Hypomangnesaemia
Idiopathic

74
Q

What is the long term management of hypoparathyroidism?

A

Calcium and Vitamin D supplements

75
Q

Describe hypomagnasaemia

A

Calcium release from cells is dependent on magnesium. In magnesium deficiency intracellular calcium is high, PTH release is inhibited which makes muscle receptors less sensitive to PTH.

76
Q

What causes hypomagnasaemia?

A

Alcohol, drugs, GI illness, pancreatitis, malabsorption

77
Q

What is pseudohypoparathyroidism?

A

Genetic defect that leads to low calcium but elevated PTH as a result of PTH resistance

78
Q

How does pseudohypoparathyroidism present?

A

Bone abnormalities, obesity, subcutaneous calcification and learning difficulties

79
Q

What is the aetiology of rickets/osteomalacia?

A
  • diet
  • malabsorption
  • chronic renal failure
  • lack of sunlight
  • drugs
80
Q

What does vitamin D deficiency cause?

A

Low calcium which leads to muscle wasting (proximal myopathy), dental defects (caries enamel), bone tenderness, fractures and deformity.

81
Q

What are the long term consequences of vitamin D deficiency?

A

Bone demineralisation/fractures, malignancy, heart disease, diabetes

82
Q

What is the treatment for vitamin D deficiency?

A

Vit D3 tablets
Calcitriol
Alfacalcidol
Adcal D3 (combined calcium and vit D3)

83
Q

How would Vit D resistant rickets present?

A

Low phosphate and high vitamin D usually due to X linked hypophophataemia

84
Q

How is vitamin D resistant rickets treated?

A

Phosphate and vitamin D supplements +/- surgery

Endocrine (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions